Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a prospective trial of 75 Chinese patients with histologically proven inoperable hepatocellular carcinoma (HCC), 25 patients were randomised to receive doxorubicin 60-75 mg m-2 intravenously once every 3 weeks, 25 to receive recombinant alpha 2 interferon (rIFN) (Roferon) 9-18 x 10(6) IU m-2 intramuscularly (i.m.) daily and 25 to receive rIFN 25-50 x 10(6) IU m-2 i.m. three times weekly. Patients were switched to the other drug if: (a) there was progressive disease after 12 weeks, (b) unacceptable toxicity developed and (c) they had received a total of 500 mg m-2 of doxorubicin. Six patients had switching over of therapy, three on doxorubicin and three on rIFN. In the remaining 69 patients on single drug therapy, the median survival rate of patients on doxorubicin and rIFN was 4.8 and 8.3 weeks respectively (P = ns.). rIFN induced tumour regression of 25-50% in 12% of patients and of over 50% in 10% of patients. When compared with doxorubicin, rIFN was associated with more tumour regression (P = 0.00199) and less progressive tumours (P = 0.00017). It caused less prolonged and less severe marrow suppression (P = 0.01217), and had significantly less fatal complications than doxorubicin (P = 0.01383). Doxorubicin caused fatal complications due to cardiotoxicity and neutropenia in 25% of patients. rIFN was associated with fatal complications due to dementia and renal failure in 3.8% of patients. In the treatment of inoperable HCC, rIFN is superior to doxorubicin in causing more tumour regression, less serious marrow suppression and less fatal complications.
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PMID:Recombinant alpha 2 interferon is superior to doxorubicin for inoperable hepatocellular carcinoma: a prospective randomised trial. 255 81

Between March 1982 and September 1983, 40 inpatients (25 men and 15 women, mean age 53 years) with alcoholic cirrhosis and total serum bilirubin greater than or equal to 5 mg per dl were studied. Those with hepatocellular carcinoma, renal failure, hyponatremia, septicemia, spontaneous bacterial peritonitis, gastrointestinal bleeding, and hepatic coma were excluded. Patients were studied for 28 days. The two groups were offered an oral diet containing 40 kcal per kg per day. Patients in the supplementary parenteral nutrition group received 40 kcal per kg per day and 200 mg nitrogen per kg per day using a central catheter. The major endpoint was total serum bilirubin on Day 28. On admission, serum bilirubin was not significantly different in the two groups: oral group, 12.5 +/- 6.6 mg per dl; supplementary parenteral nutrition group, 12.3 +/- 8.5 mg per dl. On Day 28, serum bilirubin was lower in the supplementary parenteral nutrition group (2.5 +/- 1.4 mg per dl) than in the oral group (4.1 +/- 2.2 mg per dl) (p less than 0.02). Serum bilirubin was also lower in the supplementary parenteral nutrition group than in the oral group on Days 7, 14 and 21 (p less than 0.05). Analysis of covariance, considering serum bilirubin on admission and at randomization and time between admission and randomization, confirmed these results. On Day 28, anthropometric parameters, serum transferrin, prealbumin and retinol-binding protein were higher in the supplementary parenteral nutrition group, but the differences were not significant. Serum albumin was significantly lower in the supplementary parenteral nutrition group. The incidence of encephalopathy and sepsis was not significantly different between the two groups.
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PMID:A randomized clinical trial of supplementary parenteral nutrition in jaundiced alcoholic cirrhotic patients. 308 33

We have re-evaluated the isolation and characteristics of human urinary alkaline phosphatases (ALPs). From the results of physicochemical properties and immunological identification, the urinary ALPs from healthy subjects and patients with hepatoma were found to be similar in nature to liver and/or bone-like ALP. In patients with chronic or acute nephritis, the ALPs contained a major band of kidney-like ALP with a minor band of bone and intestinal ALPs. However, the ALPs in pregnant women had not only liver and bone ALPs but also placental-like ALP. It is interesting that only bone-like ALP was detected in psychiatric patients administered chlorpromazine. In the conditions we investigated, the molecular sizes of the urinary ALPs were similar as those of original ALPs, except for the enzyme from renal failure. Moreover, the total activity of urinary ALP was closely related to the level of serum ALP, being in a ratio of 1/40. In general, urinary ALP may be derived from serum ALP by minor modification, suggesting that the identification of excreted ALP in urine is a good marker for disturbed organs in respective diseases.
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PMID:Organ specific properties for human urinary alkaline phosphatases. 328 Jan 68

To establish the impact of transplantation on the course of chronic hepatitis B liver disease we performed a prospective study of the clinical and pathological sequelae of hepatitis B disease in all 22 patients who had renal allografts that functioned for more than 1 year and who were hepatitis B surface antigen (HBsAg)-positive following transplantation. No patient converted to HBsAg-negative. During a mean follow-up of 83 months serial liver biopsies were performed in 20 patients and 1 liver biopsy was available in the remaining 2 patients. Eleven patients died of liver disease, 5 of whom died of hepatic failure, 3 with hepatoma, 2 of gastrointestinal hemorrhage, and 1 of ascites with pleuroperitoneal fistula. Aggressive liver disease was observed in the vast majority of patients: 12 ultimately developed cirrhosis, (mean follow-up 81 months), 6 chronic active hepatitis (mean follow-up 93 months), 3 chronic persistent hepatitis (mean follow-up 89 months), and in 1 patient the presence of HB virus in hepatocytes was the sole morphologic alteration (follow-up 42 months). There was a marked tendency to progression in that 82% of patients with virus only, reactive hepatitis, or chronic persistent hepatitis on initial biopsy subsequently developed chronic active hepatitis or cirrhosis. For comparison, 10 HBsAg-positive patients whose renal failure had been treated by hemodialysis were also studied over a comparable period. Four patients converted to the negative state. Biochemical evidence of persistent liver dysfunction occurred in only 1 patient and no patient has died from complications of liver disease. We conclude that in the immunosuppressed renal transplant patient HB infection often results in the development of cirrhosis, leading to death from hepatoma and hepatic failure. This course is worse than that in dialysis patients. Renal transplantation of HBsAg-positive patients with end-stage renal failure may be inadvisable.
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PMID:The impact of renal transplantation on the course of hepatitis B liver disease. 389 Feb 90

Six HBsAg negative patients with cirrhosis of the liver (CL) presented with recurrent bouts of palpable purpura in the legs due to small vessel leucocytoclastic vasculitis. In addition, all patients had renal failure, proteinuria and microhaematuria. Renal biopsy disclosed either diffuse proliferative (3 cases) or focal necrotising glomerulonephritis with crescents (2 cases). One patient had IgM-IgG mixed cryoglobulinaemia (type II). Four patients died of complications of their CL. Hepatocellular carcinoma was found in 1 case. In the patient without renal biopsy renal function improved following steroids and cyclophosphamide. The pathogenesis of this syndrome of cutaneous vasculitis with severe glomerular involvement in CL is unknown but could be immune-complex mediated.
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PMID:Renal involvement in a syndrome of vasculitis complicating HBsAg negative cirrhosis of the liver. 399 59

We developed a specific RIA for a somatomedin (Sm)-binding protein, with an approximate mol wt of 35-40,000, purified from midgestational human amniotic fluid (AF) and termed AF-binding protein (AFBP). After Sephadex G-200 chromatography AFBP-RIA activity was found in fractions of fetal and cord serum only at a kav corresponding to a mol wt of +/- 40,000. Whole serum or plasma dilutions in a range of 1:20 to 1:600 showed parallelism with the standard curve. Sm-binding activity in fetal serum was found solely at a mol wt of 30-40,000; in cord serum additionally at a mol wt range of 150-200,000. AFBP serum or plasma concentrations determined by RIA were influenced by several factors: AFBP values in eight adults were highest in the morning (mean +/- SEM, 0.7 +/- 0.1 mu geq/ml) and lowest at night (0.3 +/- 0.1). AFBP values in pre- and postnatal serum showed a gradual decline with increasing age: fetal serum: mean +/- SEM, 36.7 +/- 15.7 (n = 17); adults: 0.6 +/- 0.07 mu geq/ml (n = 19). In serum from GH-deficient children AFBP concentrations were significantly higher than in an age-matched control group (P less than 0.05). Elevated values also were found in serum of children with end-stage renal failure and in serum of pregnant women at 36 weeks of gestation. AFBP was found in urine of preterm infants (mean +/- SEM, 0.04 +/- 0.005 mu geq/ml; n = 31). AFBP immunoreactivity was demonstrable in serum of three orangoutan mothers and their three children and in medium of a hepatoma cell line (PLC/PRF/5) but not in bovine, porcine, rabbit, or rat serum or in medium of cell cultures of (pre-)term placentae. We conclude that AFBP immunoreactivity is present in pre- and postnatal serum and has striking similarity to an unsaturated serum Sm-binding protein with a mol wt of +/- 40,000.
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PMID:Immunoassay of a somatomedin-binding protein from human amniotic fluid: levels in fetal, neonatal, and adult sera. 620

Malignant disease arises more commonly in renal transplant recipients than in non-transplanted individuals. Renal polycystic disease is the only cause of renal failure that has a statistically significant association with the acquisition of malignancy in renal transplant recipients. This patient, who had renal failure due to polycystic disease, is the first reported renal transplant recipient to develop a hepatocellular carcinoma in an otherwise completely normal liver. It is suggested that patients with polycystic renal disease may have an unidentified factor that predisposes to the development of malignancy in them after transplantation.
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PMID:Primary hepatocellular carcinoma arising in a renal transplant recipient with polycystic disease. 630 48

Forty patients with hepatoma and metastatic tumors of liver were treated with rapid arterial infusion administered simultaneously using 30-40 mg of adriamycin and 10-20 mg of mitomycin C into the hepatic artery by Seldinger catheter. They were 16 patients with breast cancer, 21 with gastrointestinal tumors including hepatoma; 6, gastric cancer; 5, colon cancer; 7, gallbladder cancer; 2, pancreas cancer; 1, and three with other malignancies, respectively. Partial responses were obtained in 14 of 40 patients (35%). The response rate in patients with breast cancer was 44% (7/16), while it was 29% (6/21) with gastrointestinal tumors. The median duration of response was relatively short, being 3.5 months in the former patients and 2.3 months in the latter patients. The median duration of survival was 4.0+ months. The results indicate that this arterial infusion therapy is one of the useful treatments in the management of malignant tumors of the liver. Leukopenia less than 4 x 10(3)/cmm was seen in 63%, while thrombocytopenia less than 100 x 10(3)/cmm in 38%, and decreased hemoglobin value of more than 2 g/dl in 13%, which were quite tolerable. Gastrointestinal symptoms and hair loss were milder than those from systemic chemotherapy. Renal toxicity was seen in three patients, and two patients died of renal failure, thus the renal toxicity, which may be related to contrast media as well as anticancer agents, should be carefully prevented by proper hydration.
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PMID:[Arterial infusion of combination chemotherapy using adriamycin and mitomycin C for hepatoma and metastatic tumors of the liver]. 630 77

A prospective study of the clinical and pathological sequelae of hepatitis B disease in 22 immunosuppressed renal transplant patients is reported. All patients had allografts that functioned for more than 1 year, and all were hepatitis B surface antigen (HBsAg)-positive following transplantation. None of the 18 patients who had serial HBsAg tests converted to HBsAg negative. Serial liver biopsies were performed in 19 patients and one liver biopsy was available in the remaining three patients. Follow-up ranged from 12 to 93 months. Seven patients ultimately developed cirrhosis, 6 developed chronic active hepatitis, 5 developed chronic persistent hepatitis, and in 4 the presence of HB virus in hepatocytes was the sole morphologic alteration. The initial liver biopsy was not an accurate predictor of ultimate severity of liver disease because 5 of the 12 patients with virus only or chronic persistent hepatitis subsequently developed chronic active hepatitis or cirrhosis. Clinical liver dysfunction occurred in 8 patients, all of whom had chronic active hepatitis or cirrhosis. Three patients died with hepatic failure and 2 with hepatoma. The risk of death from liver disease in HBsAg-positive renal transplant patients was 5% per patient-year. For comparison, 10 HBsAg-positive patients whose renal failure had been treated by hemodialysis were also studied over a comparable period. Biochemical evidence of persistent liver dysfunction recurred in 1 patient only; 4 patients converted to the HBsAg-negative state; and no patient has died from complications of liver disease. We conclude that in the immunosuppressed renal transplant patient HB infection often results in the development of chronic active hepatitis, leading to cirrhosis and death from hepatoma and hepatic failure.
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PMID:The clinical and pathological course of hepatitis B liver disease in renal transplant recipients. 637 1

Bone histology and its relationship with calcium metabolism was evaluated in adult patients with nephrotic syndrome: 29 had normal renal function (GFR 103 +/- 4 ml/min/1.73 m2) (group 1) and 20 had renal insufficiency (GFR 31 +/- 4 ml/min/1.73 m2) (group 2). In group 1, serum PTH, 1.25-HCC and 24.25-HCC levels were normal, while 25-HCC values were reduced. Bone histology was normal in 76% of the patients, while 17% had isolated osteomalacia and 7% an associated bone resorption. Group 2 showed a higher incidence of bone resorption when compared with a matched group of patients with renal failure and no proteinuria (40% vs. 13%) and a comparable frequency of isolated mineralization defect (25% vs. 34%). PTH levels were definitely increased and serum total calcium and all the vitamin D metabolites were reduced. A significant correlation between the apparent duration of the disease and the severity of osteodystrophy was found only in group 2. In conclusion, no constant derangement of calcium metabolism and bone histology is evident in patients with nephrotic syndrome and normal renal function, while patients with persistent proteinuria are at high risk of osteodystrophy even in the early phases of renal failure.
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PMID:Bone histology and calcium metabolism in patients with nephrotic syndrome and normal or reduced renal function. 673 66


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